Acute myeloid leukemia is characterized by accumulation of immature myeloid progenitor cells. Leukemogenesis results from deregulation of oncogenes, tumor suppressors or transcription factors which control myeloid lineage differentiation, self-renewal and/or proliferation. The transcription factor CCAAT/enhancer binding protein alpha (C/EBPα) promotes differentiation of granulocyte and macrophages and negatively regulates hematopoietic stem cell self-renewal. During emergency granulopoiesis and during leukemogenesis C/EBPα is substituted by transcriptional activity of C/EBPβ and STAT3 transcription factors. Mutations or down-regulation of C/EBPα are frequently observed in patients with AML. Short activating RNAs (saRNAs) are capable of inducing gene expression. A factor in the clinical application of saRNA and other oligonucleotide therapeutics is difficulty in their targeted delivery, additionally complicated by the inherent sensitivity of the immune system to nucleic acids. STAT3 operates in both cancer cells and non-malignant tumor-associated cells. However, targeting transcription factors such as STAT3, is complicated by their lack of enzymatic activity and requires non-pharmacologic approaches. Antisense technology for suppressing STAT3 has limited effect because available antisense oligonucleotides lack cell selectivity. The present disclosure relates to compounds, compositions, and methods of treating cancer, e.g., AML, with saRNA conjugated phosphorothioated oligonucleotides that are stable and are suitable for systemic administration against disseminated cancers. The present disclosure also relates to compounds, compositions, and methods of treating cancer, e.g., prostate cancer and glioblastoma with antisense oligonucleotides conjugated to phosphorothioated oligonucleotides.